Jesús Egido

Universidad Autónoma de Madrid, Madrid, Madrid, Spain

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Publications (635)2814.9 Total impact

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    ABSTRACT: Diabetic cardiomyopathy is defined as ventricular dysfunction initiated by alterations in cardiac energy substrates in the absence of coronary artery disease and hypertension. In addition to the demonstrated burden of cardiovascular events associated with diabetes, diabetic cardiomyopathy partly explains why diabetic patients are subject to a greater risk of heart failure and a worse outcome after myocardial ischemia. The raising prevalence and accumulating costs of cardiovascular disease in diabetic patients underscore the deficiencies of tertiary prevention and call for a shift in medical treatment. It is becoming increasingly clearer that the effective prevention and treatment of diabetic cardiomyopathy require measures to regulate the metabolic derangement occurring in the heart rather than merely restoring suitable systemic parameters. Recent research has provided deeper insight into the metabolic etiology of diabetic cardiomyopathy and numerous heart-specific targets that may substitute or reinforce current strategies. From both experimental and translational perspectives, in this review we first discuss the progress made with conventional therapies, and then focus on the need for prospective metabolic targets that may avert myocardial vulnerability and functional decline in next-generation diabetic care.
    Cardiovascular Diabetology 12/2015; 14(1). DOI:10.1186/s12933-015-0173-8 · 3.71 Impact Factor
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    ABSTRACT: Reduced soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) levels have been related with cardiovascular disease. However, there are no data on the relationship between sTWEAK and atherosclerotic burden in subjects with or without cardiovascular risk factors but free from clinical disease. We have analyzed the association between circulating sTWEAK levels and the presence of carotid and/or femoral atherosclerotic plaques in subjects without known vascular disease.
    Atherosclerosis 04/2015; 239(2). DOI:10.1016/j.atherosclerosis.2015.01.040 · 3.71 Impact Factor
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    ABSTRACT: Abdominal aortic aneurysm (AAA) evolution is unpredictable, and there is no therapy except surgery for patients with an aortic size> 5 cm (large AAA). We aimed to identify new potential biomarkers that could facilitate prognosis and treatment of patients with AAA. A differential quantitative proteomic analysis of plasma proteins was performed in AAA patients at different stages of evolution [small AAA (aortic size=3-5cm) vs large AAA] using iTRAQ labelling, high-throughput nano-LC-MS/MS and a novel multi-layered statistical model. Among the proteins identified, ApoA-I was decreased in patients with large AAA compared to those with small AAA. These results were validated by ELISA on plasma samples from small (n=90) and large AAA (n=26) patients (150± 3 vs 133± 5 mg/dl, respectively, p< 0.001). ApoA-I levels strongly correlated with HDL-Cholesterol (HDL-C) concentration (r=0.9, p< 0.001) and showed a negative correlation with aortic size (r=-0.4, p< 0.01) and thrombus volume (r=-0.3, p< 0.01), which remained significant after adjusting for traditional risk factors. In a prospective study, HDL-C independently predicted aneurysmal growth rate in multiple linear regression analysis (n=122, p=0.008) and was inversely associated with need for surgical repair (Adjusted hazard ratio: 0.18, 95 % confidence interval: 0.04-0.74, p=0.018). In a nation-wide Danish registry, we found lower mean HDL-C concentration in large AAA patients (n=6,560) compared with patients with aorto-iliac occlusive disease (n=23,496) (0.89± 2.99 vs 1.59± 5.74 mmol/l, p< 0.001). Finally, reduced mean aortic AAA diameter was observed in AngII-infused mice treated with ApoA-I mimetic peptide compared with saline-injected controls. In conclusion, ApoA-I/HDL-C systemic levels are negatively associated with AAA evolution. Therapies targeting HDL functionality could halt AAA formation.
    Thrombosis and Haemostasis 03/2015; 113(6). DOI:10.1160/TH14-10-0874 · 5.76 Impact Factor
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    ABSTRACT: Inflammation is a main feature of progressive kidney disease. Gremlin binds to bone morphogenetic proteins (BMPs), acting as an antagonist and regulating nephrogenesis and fibrosis among other processes. Gremlin also binds to vascular endothelial growth factor receptor-2 (VEGFR2) in endothelial cells to induce angiogenesis. In renal cells, Gremlin regulates proliferation and fibrosis, but there are no data about inflammatory-related events. We have investigated the direct effects of Gremlin in the kidney, evaluating whether VEGFR2 is a functional Gremlin receptor. Administration of recombinant Gremlin to murine kidneys induced rapid and sustained activation of VEGFR2 signalling, located in proximal tubular epithelial cells. Gremlin bound to VEGFR2 in these cells in vitro, activating this signalling pathway independently of its action as an antagonist of BMPs. In vivo, Gremlin caused early renal damage, characterized by activation of the nuclear factor-κB pathway linked to up-regulation of pro-inflammatory factors and infiltration of immune inflammatory cells. VEGFR2 blockade diminished Gremlin-induced renal inflammatory responses. The link between Gremlin/VEGFR2 and NF-κB/inflammation was confirmed in vitro. Gremlin overexpression was associated to VEGFR2 activation in human renal disease and in the unilateral ureteral obstruction experimental model, where VEGFR2 kinase inhibition diminished renal inflammation. Our data show that a Gremlin/VEGFR2 axis participates in renal inflammation and could be a novel target for kidney disease. This article is protected by copyright. All rights reserved.
    The Journal of Pathology 03/2015; DOI:10.1002/path.4537 · 7.33 Impact Factor
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    ABSTRACT: Chronic activation of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway contributes to vascular inflammation and atherosclerosis by inducing expression of genes involved in cell proliferation, differentiation and migration. We aimed to investigate whether enforced expression of negative regulators, the suppressors of cytokine signaling (SOCS1 and SOCS3), inhibits harmful JAK/STAT-mediated responses and affects atherosclerosis in apolipoprotein E knockout mice. Adenovirus-mediated SOCS1 transgene expression impaired the onset and progression of atherosclerosis without impact on lipid profile, whereas SOCS3 was only effective on early atherosclerosis. Mechanistically, SOCS gene delivery, primarily SOCS1, attenuated STAT1 and STAT3 activation and reduced the expression of STAT-dependent genes (chemokine/chemokine receptors, adhesion molecules, pro-inflammatory cytokines and scavenger receptors) in aortic tissue. Furthermore, atherosclerotic plaques exhibit a more stable phenotype characterized by lower lipids, T cells and M1 macrophages and higher M2 macrophages and collagen. Atheroprotection was accompanied by a systemic alteration of T helper- and T regulatory-related genes and a reduced activation state of circulating monocytes. In vascular smooth muscle cells and macrophages, SOCS gene delivery inhibited cytokine-induced STAT activation, pro-inflammatory gene expression, cell migration and proliferation. In conclusion, targeting SOCS proteins, predominantly SOCS1, to suppress pathological mechanisms involved in atheroma plaque progression and destabilization could be an interesting anti-atherosclerotic strategy.
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    ABSTRACT: Vitamin D deficiency has been linked to many different pathologies, especially with morbimortality in patients with chronic kidney disease. The progressive loss of renal function leads to calcitriol deficiency and homeostatic changes in calcium, phosphorus, FGF-23 and PTH, among others. All these changes can also influence vitamin D receptor (VDR) activation and the development of secondary hyperparathyroidism (SHPT). The biologic actions of both vitamin D and its synthetic analogues are mediated by binding to the same VDR, acting on different genes. There is a narrow relationship between low levels of calcitriol and SHPT. The combined approach of VDR activation and phosphate restriction, among others, plays an important role in the early treatment of the chronic kidney disease-mineral and bone disorder (CKD-MBD). The Spanish Society of Nephrology, in order to reduce the uniform and significant association with CKD-associated mortality, calcidiol and high phosphate levels suggests normalization of phosphate as well as calcidiol levels in both CKD and dialysis patients. Moreover, it considers that, in addition to selective/non selective activation of VDR for the prevention and treatment of SHPT, VDR could be activated in dialysis patients by native vitamin D or even low paricalcitol doses, independently of PTH levels, as some cohort studies and a recent metaanalysis have found an association between treatment with active vitamin D and decreased mortality in patients with CKD. In general it is considered reasonable to use all this information to individualise decision making.
    Nefrologia: publicacion oficial de la Sociedad Espanola Nefrologia 01/2015; 35(1):28-41. DOI:10.3265/Nefrologia.pre2014.Sep.11796 · 1.44 Impact Factor
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    ABSTRACT: Background: A positive calcium balance may contribute to vascular calcification, while a negative balance increases iPTH. We explored the impact of different dialysate calcium concentrations on bone and mineral metabolism parameters according to pre-dialysis serum calcium levels. Results: Fifty-six hemodialysis patients were dialyzed with 3.0 or 2.5 mEq/l dialysate [calcium] in a crossover study of two weeks. Bone mineral metabolites were measured prior to and following the hemodialysis session. A 3.0 mEq/l dialysate [calcium] increased more post-dialysis total calcium and ionized calcium than 2.5 mEq/l dialysate [calcium]. The mildest dialysis-induced changes in calcium and PTH were observed in patients with pre-dialysis serum calcium <8.75 mg/dl dialyzed with 2.5 mEq/l dialysate [calcium] and in patients with pre-dialysis serum calcium >9.15 mg/dl dialyzed with 3.0 mEq/l calcium dialysate. Conclusion: In conclusion, the individualization of dialysate calcium concentration according to baseline pre-dialysis serum calcium may prevent major excursions in post-dialysis serum calcium and iPTH levels. Short Summary: High calcium dialysate may increase serum calcium in hemodialysis patients, while low dialysate calcium may increase PTH. Individualization of dialysate calcium according to predialysis serum calcium levels may prevent or decrease unwanted excursions of both serum calcium and PTH. © 2014 S. Karger AG, Basel.
    Blood Purification 12/2014; 38(3-4):224-233. DOI:10.1159/000366126 · 1.92 Impact Factor
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    ABSTRACT: Patients with coronary heart disease (CHD) without classical cardiovascular risk factors (CRFs) are uncommon, and their profile has not been thoroughly studied. In CHD patients, we have assessed the differences in several biomarkers between those with and without CRF. We studied 704 patients with CHD, analyzing plasma levels of biomarkers related to inflammation, thrombosis, renal damage, and heart failure: high-sensitivity C-reactive protein (hs-CRP), monocyte chemoattractant protein-1 (MCP-1), galectin-3, N-terminal fragment of brain natriuretic peptide (NT-pro-BNP), calcidiol (vitamin D metabolite), fibroblast growth factor-23 (FGF-23), parathormone, and phosphate. Twenty patients (2.8%) exhibited no CRFs. Clinical variables were well balanced in both groups, with the logical exceptions of no use of antidiabetic drugs, lower triglyceride and glucose, and higher high-density lipoprotein cholesterol in no-CRF patients. No-CRF patients showed lower hs-CRP (2.574±3.120 vs. 4.554±9.786mg/L; p=0.018), MCP-1 (114.75±36.29 vs. 143.56±65.37pg/ml; p=0.003), and FGF-23 (79.28±40.22 vs. 105.17±156.61RU/ml; p=0.024), and higher calcidiol (23.66±9.12 vs. 19.49±8.18ng/ml; p=0.025) levels. At follow-up, 10.0% vs. 11.0% patients experienced acute ischemic event, heart failure, or death in the non-CRF and CRF groups, respectively (p=0.815, log-rank test). The limited number of non-CRF patients may have influenced this finding. A Cox regression analysis in the whole population showed that high calcidiol, and low MCP-1 and FGF-23 plasma levels are associated with a better prognosis. CHD patients without CRFs show a favorable biomarker profile in terms of inflammation and mineral metabolism. Further studies are needed to investigate whether this difference translates into a better prognosis. Copyright © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
    Journal of Cardiology 12/2014; DOI:10.1016/j.jjcc.2014.11.006 · 2.57 Impact Factor
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    ABSTRACT: The tubular epithelium may be intrinsically involved in promoting kidney injury by junctional instability, epithelial-mesenchymal transition (EMT) and extracellular matrix remodelling. In this work, we investigated whether the pleiotropic and proinflammatory cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK), could be able to disturb junctional protein expression and to induce EMT of tubular cells. In cultured murine proximal tubular cells TWEAK induced phenotypic changes that were accompanied by F-actin redistribution, loss of epithelial adherent (E-cadherin, Cadherin-16, β-catenin) and tight junction (ZO-1) proteins, and re-expression of the mesenchymal protein Vimentin. The transcriptional repressors Snail and HNF1β were also modulated by TWEAK. In a murine model of obstructive renal pathology, TWEAK expression correlated with the appearance of the mesenchymal marker αSMA in kidney tubular cells. Mechanistically, the epithelial changes induced by TWEAK, including loss of epithelial integrity and EMT, via Fn14 were TGF-β1 independent, but mediated by several intracellular signaling systems, including the canonical NF-κB, ERK activation and the vitamin D receptor modulation.These results highlight potential contributions of TWEAK-induced inflammatory mechanisms that could unveil new pathogenic effects of TWEAK starting tubulointerstitial damage and fibrosis. This article is protected by copyright. All rights reserved
    Journal of Cellular Physiology 12/2014; DOI:10.1002/jcp.24905 · 3.87 Impact Factor
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    ABSTRACT: GLA p.(Arg118Cys) variant is associated with high residual enzyme activity•The p.(Arg118Cys) variant does not segregate with Fabry disease clinical phenotypes•The p.(Arg118Cys) variant might be a modulator of the multifactorial risk of cerebrovascular disease•The Cys118 allelic frequency in the Portuguese population has been estimated as 0.001
    Molecular Genetics and Metabolism 11/2014; 114(2). DOI:10.1016/j.ymgme.2014.11.004 · 2.83 Impact Factor
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    ABSTRACT: The nuclear factor-κB (NF-κB) is an important regulator of the inflammatory response. Angiotensin II (Ang II) activates the NF-κB pathway linked to renal inflammation. Although both AT1 and AT2 receptors are involved in Ang II-mediated NF-κB activation, the biological processes mediated by each receptor are not fully characterized. Interleukin-1β (IL-1β) is an important macrophage-derived cytokine that regulates immune and inflammatory processes, activating intracellular pathways shared with Ang II, including the NF-κB.
    Journal of Renin-Angiotensin-Aldosterone System 10/2014; DOI:10.1177/1470320314551564 · 2.27 Impact Factor
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    ABSTRACT: Background: End-stage renal disease (ESRD) conveys high mortality risk by complex mechanisms not fully elucidated but possibly linked to hormonal abnormalities, including cortisol. Whereas a high serum cortisol level has recently been linked with increased mortality in the general population, there is scarce information on the clinical associates and prognostic value of cortisol levels in ESRD. Patients and methods: Prospective study of prevalent hemodialysis patients (n = 75), mostly non-diabetic (76%), where cortisol levels were assessed and patients were afterwards followed for a median of 20 (interquartile range (IQR) 8 - 31) months. Results: Cortisol levels were negatively correlated with plasma sodium (Rho = -0.26. p < 0.025) and positively correlated with C-reactive protein (CRP; Rho = 0.26, p = 0.027). The association with CRP remained independent of multiple confounders. Baseline cortisol levels of those who died were higher than of those who survived (19.8 ± 6.9 vs. 15.3 ± 5.7 mcg/dL, p = 0.0083). Kaplan-Meier analysis showed that patients with cortisol levels within the highest tertile (≥ 18 mcg/dL) were at increased risk of death. Cortisol was associated with risk of death both in crude and adjusted Cox proportional hazards models (HR 1.09 (1.021 - 1.167) p = 0.011; and 1.16 (1.027 - 1.309), p = 0.01, respectively)). Conclusions: High serum concentrations of cortisol were associated with a state of inflammation and independently identified a subgroup of chronic hemodialysis patients at a high mortality risk.
    Clinical nephrology 10/2014; 82 (2014)(4):247-256. DOI:10.5414/CN108311 · 1.23 Impact Factor
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    ABSTRACT: At present, there is no tool validated by scientific societies for risk stratification of patients with stable coronary artery disease (SCAD). It has been shown that plasma levels of monocyte chemoattractant protein-1 (MCP-1), galectin-3 and pro-B-type natriuretic peptide amino-terminal (NT-proBNP) have prognostic value in this population.
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    ABSTRACT: Introduction At present, there is no tool validated by scientific societies for risk stratification of patients with stable coronary artery disease (SCAD). It has been shown that plasma levels of monocyte chemoattractant protein-1 (MCP-1), galectin-3 and pro-B-type natriuretic peptide amino-terminal (NT-proBNP) have prognostic value in this population. Objetive To analyze the prognostic value of a clinical risk scale published in Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study and determining its predictive capacity when combined with plasma levels of MCP-1, galectin-3 and NT-proBNP in patients with SCAD. Methods and results A total of 706 patients with SCAD and a history of acute coronary syndrome (ACS) were analyzed over a follow up period of 2.2 ± 0.99 years. The primary endpoint was the occurrence of an ischemic event (any SCA, stroke or transient ischemic attack), heart failure, or death. A clinical risk scale derived from the LIPID study significantly predicted the development of the primary endpoint, with an area under the ROC curve (Receiver Operating Characteristic) of 0.642 (0.579 to 0.705); P < 0.001. A composite score was developed by adding the scores of the LIPID and scale decile levels of MCP -1, galectin -3 and NT-proBNP. The predictive value improved with an area under the curve of 0.744 (0.684 to 0.805); P < 0.001 (P = 0.022 for comparison). A score greater than 21.5 had a sensitivity of 74% and a specificity of 61% for the development of the primary endpoint (P < 0.001, log -rank test). Conclusion Plasma levels of MCP-1, galectin -3 and NT-proBNP improve the ability of the LIPID clinical scale to predict the prognosis of patients with SCAD.
    Clínica e Investigación en Arteriosclerosis 08/2014; DOI:10.1016/j.arteri.2014.06.003
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    ABSTRACT: Aims: Connective tissue growth factor (CTGF/CCN2) is a developmental gene upregulated in pathological conditions including cardiovascular diseases, whose product is a matricellular protein that can be degraded to biologically active fragments. Among them, the C-terminal module IV (CCN2(IV)) regulates many cellular functions, but there is no data about redox-process. Therefore, we investigated whether CCN2(IV) through redox signaling regulates vascular responses. Results: CCN2(IV) increased superoxide anion production (O2.-) in murine aorta (ex vivo and in vivo) and in cultured vascular smooth muscle cells (VSMCs). In isolated murine aorta CCN2(IV), via O2.-, increased phenylephrine-induced vascular contraction. CCN2(IV) in vivo regulated several redox-related processes in mice aorta, including increased Nox1 activity, protein nitrosylation, endothelial dysfunction and activation of the NF-κB pathway and its related proinflammatory factors. The role of Nox1 in CCN2(IV)-mediated vascular responses in vivo was investigated by gene silencing. Administration of a Nox1 morpholino diminished aortic O2.- production, endothelial dysfunction, NF-κB activation and overexpression of proinflammatory genes in CCN2(IV)-injected mice. The link CCN2(IV)/Nox-1/NF-κB/inflammation was confirmed in cultured VSMCs. Epidermal growth factor receptor (EGFR) is a known CCN2 receptor. In VSMCs CCN2(IV) activates EGFR signaling. Moreover, EGFR kinase inhibition blocked vascular responses in CCN2(IV)-injected mice. Innovation and conclusion: CCN2(IV) is a novel pro-oxidant factor that in VSMCs induces O2.- production via EGFR/Nox1 activation. Our in vivo data demonstrate that CCN2(IV) through EGFR/Nox1 signaling pathway induces endothelial dysfunction and activation of the NF-κB inflammatory pathway. Therefore, CCN2(IV) could be considered as a potential therapeutic target for redox-related cardiovascular diseases.
    Antioxidants and Redox Signaling 07/2014; 22(1). DOI:10.1089/ars.2013.5500 · 7.67 Impact Factor
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    ABSTRACT: A growing number of patients are recognized worldwide to have chronic kidney disease. Glomerular and interstitial fibrosis are hallmarks of renal progression. However, fibrosis of the kidney remains an unresolved challenge, and its molecular mechanisms are still not fully understood. Gremlin is an embryogenic gene that has been shown to play a key role in nephrogenesis, and its expression is generally low in the normal adult kidney. However, gremlin expression is elevated in many human renal diseases, including diabetic nephropathy, pauci-immune glomerulonephritis and chronic allograft nephropathy. Several studies have proposed that gremlin may be involved in renal damage by acting as a downstream mediator of TGF-β. To examine the in vivo role of gremlin in kidney pathophysiology, we generated seven viable transgenic mouse lines expressing human gremlin (GREM1) specifically in renal proximal tubular epithelial cells under the control of an androgen-regulated promoter. These lines demonstrated 1.2- to 200-fold increased GREM1 expression. GREM1 transgenic mice presented a normal phenotype and were without proteinuria and renal function involvement. In response to the acute renal damage cause by folic acid nephrotoxicity, tubule-specific GREM1 transgenic mice developed increased proteinuria after 7 and 14 days compared with wild-type treated mice. At 14 days tubular lesions, such as dilatation, epithelium flattening and hyaline casts, with interstitial cell infiltration and mild fibrosis were significantly more prominent in transgenic mice than wild-type mice. Tubular GREM1 overexpression was correlated with the renal upregulation of profibrotic factors, such as TGF-β and αSMA, and with increased numbers of monocytes/macrophages and lymphocytes compared to wild-type mice. Taken together, our results suggest that GREM1-overexpressing mice have an increased susceptibility to renal damage, supporting the involvement of gremlin in renal damage progression. This transgenic mouse model could be used as a new tool for enhancing the knowledge of renal disease progression.
    PLoS ONE 07/2014; 9(7):e101879. DOI:10.1371/journal.pone.0101879 · 3.53 Impact Factor
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: To study the effect of sitagliptin on glucose and fatty-acids uptake in the myocardium of type-II diabetic rats.
    Cardiovascular Research 07/2014; 103(suppl 1):S28. DOI:10.1093/cvr/cvu082.99 · 5.81 Impact Factor
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    ABSTRACT: The presence of malnutrition in chronic kidney disease (CKD) is well-known. The discovery in the last 15 years of pathophysiological mechanisms that lead to this process, such as anorexia, the increase of protein catabolism and inflammation, has created the need for a new name by the International Society of Renal Nutrition and Metabolism (ISRNM): protein-energy wasting syndrome (PEW). This document’s objectives are to propose the use of the term “desgaste proteico energético” (DPE) as a more accurate translation of the English term and to update the pathogenic mechanisms involved that are inherent to DPE (PEW). We simultaneously review the latest epidemiological evidence that highlight the relevance of malnutrition and its impact both on mortality and morbidity in CKD. Finally, we point out the need to redefine DPE (PEW) diagnostic criteria so that they are applicable to the Spanish population with CKD. We do not think that the criteria established by the ISRNM can be extrapolated to different populations, as is the case, for example, with interracial anthropometric differences.
    Nefrologia: publicacion oficial de la Sociedad Espanola Nefrologia 07/2014; 34(4):507-519. DOI:10.3265/Nefrologia.pre2014.Apr.12522 · 1.44 Impact Factor
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    ABSTRACT: Interaction of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) with its receptor Fn14 accelerates atherosclerotic plaque development in ApoE deficient mice (ApoE KO). In this work, an analysis has been made on the effect of an HMG-CoA reductase inhibitor, atorvastatin, on atherosclerotic plaque development accelerated by TWEAK in ApoE KO mice.
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    ABSTRACT: Activation of Janus kinase/signal transducers and activators of transcription (STAT) pathway by hyperglycemia and dislypidemia contributes to the progression of diabetic complications, including atherosclerosis. Suppressors of cytokine signaling (SOCS) negatively regulate Janus kinase/STAT and have emerged as promising target for anti-inflammatory therapies. We investigated whether a cell-permeable lipopeptide corresponding to the kinase inhibitory region of SOCS1 could reduce atherosclerosis in diabetic mice and identified the mechanisms involved.
    Arteriosclerosis Thrombosis and Vascular Biology 07/2014; 34(9). DOI:10.1161/ATVBAHA.114.304144 · 5.53 Impact Factor

Publication Stats

16k Citations
2,814.90 Total Impact Points

Institutions

  • 1982–2015
    • Universidad Autónoma de Madrid
      • Enfermería de la Fundación Jiménez Díaz
      Madrid, Madrid, Spain
  • 1977–2015
    • Fundación Jiménez Díaz
      • Servicio de Nefrología e Hipertensión
      Madrid, Madrid, Spain
  • 2014
    • Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas
      Barcino, Catalonia, Spain
  • 2013
    • Hospital Universitari Arnau de Vilanova
      Lérida, Catalonia, Spain
  • 2003–2013
    • Complutense University of Madrid
      Madrid, Madrid, Spain
  • 2010
    • Hospital de Santa Maria
      Lisboa, Lisbon, Portugal
    • Instituto de Investigación Sanitaria
      Madrid, Madrid, Spain
  • 2009
    • Hospital Clínic de Barcelona
      Barcino, Catalonia, Spain
  • 2008
    • Karolinska Institutet
      • Department of Clinical Science, Intervention and Technology
      Solna, Stockholm, Sweden
  • 2007
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 2006–2007
    • University of Florence
      Florens, Tuscany, Italy
  • 2004–2006
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
  • 2005
    • Klinički centar Niš
      Nisch, Central Serbia, Serbia
  • 2000–2003
    • Universidad Austral de Chile
      Ciudad de Valdivía, Los Ríos, Chile
  • 2001–2002
    • Hospital Clínico San Carlos
      Madrid, Madrid, Spain
    • Hospital Universitario Fundacion Alcorcon
      • Departamento de Cardiología
      Madrid, Madrid, Spain
  • 1992
    • Spanish National Research Council
      Madrid, Madrid, Spain
  • 1987–1989
    • Hospital Universitario Ramón y Cajal
      Madrid, Madrid, Spain